The Journal of Thoracic and Cardiovascular Surgery, Vol 106, 346-356, Copyright © 1993 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
Effects of crossclamping the descending aorta on the high-energy phosphates of myocardium and skeletal muscle. A phosphorus 31-nuclear magnetic resonance study
JA Balschi, T Henderson, EL Bradley and S Gelman
Center for NMR Research and Development, University of Alabama, Birmingham.
The study was designed to test the hypothesis that a moderate decrease in
upper body oxygen consumption observed during crossclamping of the thoracic
aorta represents tissue hypoxia (possibly as a result of microcirculatory
disorders) and results in adenosine triphosphate homeostasis disturbances.
We averaged phosphorus 31-nuclear magnetic resonance spectroscopy
measurements for 10 minutes with the use of a surface coil on the left
ventricle and on the deltoid muscle during a 1- hour period before aortic
crossclamping, during aortic crossclamping, and after aortic unclamping.
Skeletal muscle creatine phosphate levels decreased 3.1% (p < 0.01),
whereas the ratio of creatine phosphate to adenosine triphosphate decreased
2.2% (p < 0.05); glycolytic intermediates increased 70% (p < 0.01)
and intracellular inorganic phosphate decreased 9% (p < 0.01).
Myocardial creatine phosphate decreased 15% (p < 0.01), whereas the
ratio of creatine phosphate to adenosine triphosphate decreased 5.3% (p
< 0.01); glycolytic intermediates did not change, but intracellular
inorganic phosphate almost doubled (p < 0.05). These data suggest that
observations of reduced upper body oxygen consumption after aortic
crossclamping are consistent with the effects of skeletal muscle hypoxia.
Changes in myocardial metabolites may result from transient ischemia caused
by the increased wall stress.
